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The article describes the clinical case of a patient with multi-organ failure and ischemic colitis secondary to magnesium poisoning, due to the chronic intake of a parapharmacy product, used for the treatment of chronic constipation. The clinical case is described and a review of the literature is made.

Object: To present a series of ruptured cerebral aneurysms in consecutive non-selected patients treated with endovascular therapy, analyzing the initial degree of occlusion, its anatomical evolution mid-term and the variables that could statistically affect them., Methods: 251 aneurysms were first treated with coiling (embolization). 203 patients were followed up with conventional angiography for 6-8 months after the initial treatment and 182 were followed up with three-dimensional time of flight MR angiography at 18-24 months. Postoperative and mid-term anatomical results were evaluated anonymously and independently using the modified Montreal Scale., Results: The initial rate of complete occlusion was 70.9%, with rates of neck remnants and aneurysm remants of 18.3% and 10.7%, respectively. The recurrence rate was 13% after 6 months and 2% between 6 months and 2 years. The rate of retreatment was 11%. Statistically, the variables that were found to be related to the initial degree of occlusion were the use of a remodeling balloon technique (p=0.012), the size of the aneurysm neck (p=0.044) and the size of the aneurysm (p=0.004). The recanalization rate at mid-term depended on the size of the aneurysm. Although aneurysms with partial occlusion initially tended to evolve to a worse degree of closure than those with complete occlusion initially, the relationship was not statistically significant (p=0.110)., Conclusions: Embolized aneurysms can develop a worse degree of closure even when the initial occlusion is complete. The degree of occlusion depends directly on morphological factors and the use of balloon-assisted techniques. The recanalization rate at mid-term depends on the size of the aneurysm and probably on the density of the packing achieved with the initial treatment., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/)

Background: Brain death (BD) causes hemodynamic and neuroendocrine alterations including a catecholamine surge, which in turn causes histologic lesions in cardiac muscle such as contraction bands, focal mononuclear cell infiltrates and cardiomyocyte necrosis. These changes are likely to compromise heart function and could therefore also affect the graft response after heart transplantation. This study was designed to examine the catecholamine surge, the catecholamine release pattern and the histologic lesions traditionally described as characteristic of BD in hearts procured from BD donors., Methods: After BD diagnosis, specimens were taken from the left ventricle (n = 50) for histologic examination. Arterial blood samples were collected from 40 of the donors at different time-points (1 hour before BD; on BD diagnosis; and 1, 2, 3 and 4 hours after BD) to determine catecholamine levels by high-performance liquid chromatography (HPLC)., Results: The three hormones examined showed above-normal levels (epinephrine 2.36-fold, norepinephrine 8.56-fold, dopamine 54.76-fold). Release patterns included epinephrine and dopamine peaks at the time of BD and a norepinephrine peak 1 hour later. Fifty percent of the BD donors showed contraction bands and 62% displayed cardiomyocyte necrosis, which was associated with focal mononuclear cell infiltrates in 18% of cases. In 40% of donors, colocalized apoptotic and necrotic damage was observed., Conclusions: Differing extents of BD-associated cardiac lesions were observed in the donors, and >50% also showed apoptotic damage. The expected catecholamine peak at the time of BD was only detected for epinephrine and dopamine. Hormone increases were below those described in the literature, except for dopamine.

Background: Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors., Methods: Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1alpha gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement., Results: Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P<0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student's t test, P<0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death., Conclusion: Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.

Non-aneurismatic spontaneous cerebral hemorrhage or intracranial hemorrhage accounts for 10-15% of total cerebral vascular accidents. Depending on its site it can may be intraparenchymal or intraventricular. The most frequent location is in the basal ganglia and its predominant etiology is poorly-controlled arterial hypertension. In Spain, the incidence of intracerebral hemorrhage is estimated to be 15 cases per 100,000 population/ year, this being more frequent in males over 55 years old. Intracranial hemorrhage is less frequent than ischemic stroke, but has higher mortality and morbidity, it being one of the first causes of severe disability. Cerebral hemorrhage is not a monophasic phenomenon which abates immediately, because the hematoma continues to increase in the first 24 hours. Due to this reason and because of their characteristics of the disease itself, these are critical patients who must be admitted in to Intensive Care Unit where hemodynamic and cardiorespiratory control should be made as well as strict monitoring of the awareness level and remaining neuromonitoring standard parameters. In this paper, we review some aspects of the epidemiology, physiopathology, clinical presentation, diagnosis and the different therapeutic options, performing an up-date on the treatment of intracranial hemorrhage from both the medical and surgical point of view.